Implications of compromised zinc status on bone loss associated with chronic inflammation in C57BL/6 mice

Chongwatpol, Pitipa; Rendina-Ruedy, Elizabeth; Stoecker, Barbara J.; Clarke, Stephen; Lucas, Edralin A.; Smith, Brenda J.

doi:10.2147/jir.s82261

Cited by 5 publications

(2 citation statements)

References 49 publications

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“…2, 59 Chongwatpol P. et al, (2015) illuminated that LPS substantially decreased trabecular bone volume, lumbar vertebra bone mineral density, and the number of the vertebral bodies in the mouse model. 60…”

Section: And Probiotics Bacterial Species Has a Beneficial Function On Bone Mass Function (Table-1)mentioning

confidence: 99%

The role of gut microbiota in bone homeostasis

Behera

Ison

Tyagi

et al. 2020

Bone

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The gut microbiota (GM) is referred to as the second gene pool of the human body and a commensal, symbiotic, and pathogenic microorganism living in our intestines. The knowledge of the complex interaction between intestinal microbiota and health outcomes is a novel and rapidly expanding the field. Earlier studies have reported that the microbial communities affect the cellular responses and shape many aspects of physiology and pathophysiology within the body, including muscle and bone metabolism (formation and resorption). GM influences the skeletal homeostasis via affecting the host metabolism, immune function, hormone secretion, and the gut-brain axis. The premise of this review is to discuss the role of GM on bone homeostasis and skeletal muscle mass function. This review also opens up new perspectives for pathophysiological studies by establishing the presence of a 'microbiota-skeletal' axis and raising the possibility of innovative new treatments for skeletal development.

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Section: And Probiotics Bacterial Species Has a Beneficial Function On Bone Mass Function (Table-1)mentioning

confidence: 99%

The role of gut microbiota in bone homeostasis

Behera

Ison

Tyagi

et al. 2020

Bone

View full text Add to dashboard Cite

show abstract

“…These bacteria have the ability to release LPS, with small amounts entering the bloodstream normally through the gut epithelium [30]. Some of the previous studies showed that trabecular bone structures, bone mineral density, and bone strength were adversely affected by LPS treatment [32][33][34][35][36][37]. Therefore, inflammatory effects and genotoxic stress may occur in osteocyte cells exposed to LPS for a long time.…”

Section: Introductionmentioning

confidence: 99%

Verbascoside Inhibits/Repairs the Damage of LPS-Induced Inflammation by Regulating Apoptosis, Oxidative Stress, and Bone Remodeling

Akyer,

Karagur,

Ata

et al. 2023

CIMB

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Osteocytes play an important role as regulators of both osteoclasts and osteoblasts, and some proteins that are secreted from them play a role in bone remodeling and modeling. LPS affects bone structure because it is an inflammatory factor, despite verbascoside’s potential for bone preservation and healing. Osteocytes may also be involved in the control of the bone’s response to immunological changes in inflammatory situations. MLO-Y4 cells were cultured in either supplemented -MEM alone with a low serum to inhibit cell growth or media with LPS (10 ng/mL) and/or verbascoside (50 g/mL) to show the LPS effect. In our research, LPS treatment increased RANKL levels while decreasing OPG and RUNX2 expression. Treatment with verbascoside reduced RANKL expression. In our work, verbascoside increased the expression of OPG and RUNX2. In MLO-Y4 cells exposed to verbascoside, SOD, CAT, and GSH activities as well as the expression levels of bone mineralization proteins like PHEX, RUNX2, and OPG were all elevated.

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Lipopolysaccharide-Induced Bone Loss in Rodent Models: A Systematic Review and Meta-Analysis

Bott

Feldman

Comelli

et al. 2020

Journal of Bone and Mineral Research

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Osteoporosis has traditionally been characterized by underlying endocrine mechanisms, though evidence indicates a role of inflammation in its pathophysiology. Lipopolysaccharide (LPS), a component of gram‐negative bacteria that reside in the intestines, can be released into circulation and stimulate the immune system, upregulating bone resorption. Exogenous LPS is used in rodent models to study the effect of systemic inflammation on bone, and to date a variety of different doses, routes, and durations of LPS administration have been used. The study objective was to determine whether systemic administration of LPS induced inflammatory bone loss in rodent models. A systematic search of Medline and four other databases resulted in a total of 110 studies that met the inclusion criteria. Pooled standardized mean differences (SMDs) and corresponding 95% confidence intervals (CI) with a random‐effects meta‐analyses were used for bone volume fraction (BV/TV) and volumetric bone mineral density (vBMD). Heterogeneity was quantified using the I2 statistic. Shorter‐term (<2 weeks) and longer‐term (>2 weeks) LPS interventions were analyzed separately because of intractable study design differences. BV/TV was significantly reduced in both shorter‐term (SMD = −3.79%, 95% CI [−4.20, −3.38], I2 62%; p < 0.01) and longer‐term (SMD = −1.50%, 95% CI [−2.00, −1.00], I2 78%; p < 0.01) studies. vBMD was also reduced in both shorter‐term (SMD = −3.11%, 95% CI [−3.78, −2.44]; I2 72%; p < 0.01) and longer‐term (SMD = −3.49%, 95% CI [−4.94, −2.04], I2 82%; p < 0.01) studies. In both groups, regardless of duration, LPS negatively impacted trabecular bone structure but not cortical bone structure, and an upregulation in bone resorption demonstrated by bone cell staining and serum biomarkers was reported. This suggests systemically delivered exogenous LPS in rodents is a viable model for studying inflammatory bone loss, particularly in trabecular bone. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

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Implications of compromised zinc status on bone loss associated with chronic inflammation in C57BL/6 mice

Cited by 5 publications

References 49 publications

The role of gut microbiota in bone homeostasis

The role of gut microbiota in bone homeostasis

Verbascoside Inhibits/Repairs the Damage of LPS-Induced Inflammation by Regulating Apoptosis, Oxidative Stress, and Bone Remodeling

Lipopolysaccharide-Induced Bone Loss in Rodent Models: A Systematic Review and Meta-Analysis

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